The alexithymic brain: the neural pathways linking alexithymia to physical disorders

Abstract

Alexithymia is a personality trait characterized by difficulties in identifying and describing feelings and is associated with psychiatric and psychosomatic disorders. The mechanisms underlying the link between emotional dysregulation and psychosomatic disorders are unclear. Recent progress in neuroimaging has provided important information regarding emotional experience in alexithymia. We have conducted three brain imaging studies on alexithymia, which we describe herein. This article considers the role of emotion in the development of physical symptoms and discusses a possible pathway that we have identified in our neuroimaging studies linking alexithymia with psychosomatic disorders. In terms of socio-affective processing, alexithymics demonstrate lower reactivity in brain regions associated with emotion. Many studies have reported reduced activation in limbic areas (e.g., cingulate cortex, anterior insula, amygdala) and the prefrontal cortex when alexithymics attempt to feel other people's feelings or retrieve their own emotional episodes, compared to nonalexithymics. With respect to primitive emotional reactions such as the response to pain, alexithymics show amplified activity in areas considered to be involved in physical sensation. In addition to greater hormonal arousal responses in alexithymics during visceral pain, increased activity has been reported in the insula, anterior cingulate cortex, and midbrain. Moreover, in complex social situations, alexithymics may not be able to use feelings to guide their behavior appropriately. The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation. When alexithymics perform the IGT, they fail to learn an advantageous decision-making strategy and show reduced activity in the medial prefrontal cortex, a key area for successful performance of the IGT, and increased activity in the caudate, a region associated with impulsive choice. The neural machinery in alexithymia is therefore activated more on the physiologic, motor-expressive level and less in the cognitive-experiential domains of the emotional response system. Affects may play an important role in alleviating intrinsic physiologic reactions and adapting to the environment. Deficient development of emotional neural structures may lead to hypersensitivity to bodily sensations and unhealthy behaviors, a possible mechanism linking alexithymia to psychosomatic disorders.

Figure 1

A: Schema for the five levels of emotional awareness model of Lane and Schwartz[80], Parallels in the hierarchical organization of emotional experience and its neural substrates. The shell structure is intended to convey that each succeeding level adds to and modulates lower levels but does not replace them. Although each model contains five levels, a one-to-one correspondence between each level in the psychological and neuroanatomical models is not intended. Lower levels with white background correspond to implicit processes. Higher levels with gray background correspond to explicit processes. B: Neural machinery characterized by neuroimaging studies on alexithymia. Alexithymics showed weak responses in structures of highly cognitive stages, such as the capacity to feel other’s emotional reactions (socio-affective processing), and stronger responses in primitive stages such as hypersensitivity to visceral pain (interoceptive aroursal). Consequently alexithymics experience inflexible cognitive regulation, owing to impairment of the emotional guiding system. ACC = Anterior cingulate cortex; vmPFC = ventromedial prefrontal cortex.